Intergrative Session: Dive and Climb Flashcards
What mechanisms increase the diffusing capacity of the lungs with acclimatization to high altitude
Fick’s Law: want to ↑SA, ↑P1-P2 (by ↑P1 and/or ↓P2)
↑VE (more alveoli ventilated) ↑SA
Open and dilate pulmonary capillaries = ↑SA , ↑pulmonary artery pressure (but would ↑T if ↑PAP promotes oedema)
↑blood volume ↑SA
↑HCT & ↑[Hb] ↑blood O2 carry capacity, helps ↑P1-P2 by ↓P2
Pulmonary angiogenesis ↑SA
Climber Kent has just arrived at Mt Everest base camp after the 3 day trek from the nearest village. What acid-base disturbance would he mostly be experiencing on his initial rapid ascent to high altitude and explain why?
Respiratory Alkalosis
↓PB ↓PiO2 ↓PAO2 ↓PaO2 stimulates hyperventilation (↑ VE relative to VO2) ↓PaCO2 which ↓arterial H+
B = barometric i = inspired A = Alveolar a = arterial
MOVES THE EQUATION LEFT:
CO2 + H2O <–> H2CO3<–> H+ + HCO3
What compensation mechanism would be employed in response to the altitude induced acid base disturbance?
Renal retention of H+, and↑secretion of HCO3
↑removal of HCO3-leads to diuresis & dehydration unless adequate ↑ fluid intake
A headache at altitude isn’t always altitiude sickness/high altitude cerebral edema, dehydration also likely.
Headache at altitude without significant altitude gain (<500m/day) and no other AMS symptoms: drink 1L H2O (or electrolytes), take ibuprofen, wait 30 mins and reassess, i.e. correct dehydration
Acetazolamide (Diamox) can used to prevent & reduce the symptoms of altitude sicknesswhen rapid ascent is unavoidable. What is its mechanism of action and how would it help to reduce the symptoms of altitude sickness?
Acetazolamide (Diamox): inhibits carbonic anhydrase, ↓reabsorption of HCO3- in PCT thus facilitates renal loss of HCO3-. By ↓respiratory alkalosis induced by hypocapnia, it helps to facilitate ↑ ventilation by mitigating hypocapnic loss of central respiratory drive
Describe the breathing pattern commonly detected during sleep at high altitude and describe the mechanism(s) that underpins this breathing pattern
Cheyne-Stokes Respiration (describe pattern - its in picture)
High altitude:
Hypoxia causes hypoxemia (low blood O2) •
Stimulates VRG & DRG via peripheral chemoreceptors (weak but fast) to ↑VE •
Hyperventilation PaO2 and PaCO2 (pH) •
PaCO2 (pH) ↓VE via central chemoreceptors via RTN neurons (slow but strong) •
Problem exists because there are 2 competing signals (hypoxic stimulation and simultaneous hypocapnic depression) and there is ↑ lag time between changes in lung gases and central chemoreceptor response
Describe the feedback loop involved in the cough reflex
Reflex mechanism • rids the respiratory tract of any irritant that enters through the air and less frequently any fluids (drinks) and solids (food) • Can be initiated voluntarily but lacks the force and pressure as when triggered by the cough reflex
Cough receptors: rapidly adapting receptors at pharynx, trachea (carina), bronchi and bronchioles •
Afferent nerves: vagus and glossopharyngeal •
Control Centre: cough centre in medulla •
Efferent nerves: vagus, phrenic and spinal motor •
Effector muscles: glottis, external intercostals, diaphragm, major inspiratory and expiratory muscles
Describe the sequence of events involve in a cough
Inspiratory phase: Deep and sudden inhalation fills the lungs with up to 2.5 liters of air
Compression phase: The epiglottis closes and the vocal cords contract to close the larynx fully The abdominal muscles contract with force and push against the diaphragm Simultaneous forceful contraction of accessory muscles of expiration ↑ pulmonary pressure
Expiratory Phase: When pressure is sufficiently high, the vocal cords relax and the epiglottis suddenly opens ↑pulmonary pressure rushes out almost in an explosive manner The pressure also causes the bronchi and parts of the trachea to narrow to form slits through which the high airflow rate can sweep out any irritants
How can the trachea act to increase the velocity of expiratory air during a cough?
• Contraction of the trachealis muscle ↓ trachea diameter •
↑ air velocity further and aids mucus (obstruction) clearance
Climber Kent returns to Everest base camp after successfully summiting Everest for the 2nd time in a week. He has lost a considerable amount of weight, has a weak, hoarse voice and complains of fatigue and a very sore throat. On examination at HRA clinic at base camp he was found to have a persistent dry cough, Hbsat 77%, absent breath sounds and no peripheral cyanosis.
Are Kent’s symptoms consistent with a presentation of HAPE?
What is the diagnosis?
If cough is dry and %Hbsat is normal (for that altitude) then HAPE unlikely HAPE - %Hbsat for altitude, productive cough, abnormal breath sounds, peripheral cyanosis)
Khumbu cough
If Kent was suffering from HAPE, explain step by step the development of this condition and the resulting decrease in gas exchange efficiency?
HAPE = High altitude pulmonary edema
High altitude = ↓barometric pressure (PB) = PiO2 PAO2
↓PAO2 diffusion ax respiratory membrane = PaO2 (A-a diff = normal)
Induces pulmonary hypoxic vasoconstriction, which pulmonary arterial pressure (PAP)
PAP hydrostatic pressure in pulmonary artery beyond the capacity for fluid reabsorption by venous and lymphatic systems •Fluid build up in the lungs = pulmonary oedema •Oedema thickness of the respiratory membrane and further the efficiency of gas exchange
CURE: descend to lower altitudes
David (unfit dad) and young son go diving. At 150 feet jack notices david is acting weird.
What is the likely cause (and mechanism) of David’s odd behaviour?
How should Jack respond to this situation? If he did not respond, what issues may have arisen?
Both David and his son are diving at the same depth breathing the same air mixture, why might David be more likely to be at risk of DCS?
– Nitrogen Narcosis – N2 at ↑P dissolves in cell membranes. Alters the ionic conductance of neuron membranes and ↓ neuronal excitability
– Ascend immediately (with decompression stops if required and safe to do so) – If not, run out of air and may have make a rapid ascent – Nitrogen Narcosis could worsen if doesn’t ascend
–Nitrogen ~5x more soluble in fat –Not likely to affect level of nitrogen narcosis
How does hyperbaric treatment help with the problems associated with decompression illness?
High pressure will compress the N2 bubbles (↑Pressure ↓volume - link to Boyles Law) and prevent them from blocking vessels. Pressure can then be reduced slowly, allowing N2 to be removed slowly without large bubble formation.
Girl is running low on air at the end of dive and cuts her safety decompression stops short. On surfacing, Fatimah is in severe discomfort, is unable to stand properly. She has sub sternum pain worsening with deep inspirations, dyspnoea and cough. She collapses and becomes comatose. After appropriate treatment, she feels fine.
What is the likely explanation for Fatimah’s condition?
What treatment is Fatimah likely to have been given?
- –Decompression Sickness
- Arterial gas embolism
- Chokes
- CAGE (cerebral artery gas embolism)
– Immediate Oxygen (100% preferred) – Decompression Chamber (Hyperbaric Therapy)
Which organs/structures in the body are going to be susceptible to the barotrauma associated with diving?
Any gas filled spaces/organs, including the lungs, middle/inner ears, sinuses, nasal passages and the interior of hollow organs (stomach and intestines) Pulmonary barotrauma (pulmonary over pressurization syndrome, POPS, or burst lung) can occur if the diver fails to expel air from the lungs during ascent. As the diver ascends, ↓P = ↑ volume of gas in the lung
What are some contraindications for SCUBA diving?
And why are these contraindicated?
- Lung conditions
- Asthma
- Lung cysts
- Previous spontaneous pneumothorax
- Obstructive lung disease
- Lungs which empty unevenly (X-ray appearance)
- Previous thoracotomy
Any condition that impedes expiration/lung emptying and/or increases risk of lung rupture Obstructive conditions – prolonged time for expiration due to increased airway resistance and dynamic airway collapse on expiration
what is boyles and henrys law and what occurs with them during diving
boyles: inverse relationship between gas volume and pressure (increase depth underwater = increase barometric pressure which decrease volume of any gas
Henrys law: amount of gas dissolved in a solution at a given temperuature depends on the partial pressure and solubility of that gas. Increase pressure –> increase dissolved gas
How can diving cause acute oxygen poisoning
↑PAO2 = ↑ PO2 dissolved in plasma (↑PaO2) •
At very ↑PaO2, so much O2 is dissolved in blood (not bound to Hb) that O2 may be delivered to tissues solely from dissolved O2 and not from Hb bound O2, thus bypassing the Hb “buffering effect” •
Partial pressure gradient from blood to tissue (i.e. tissue metabolic rate) no longer controlling O2 delivery – excess O2 can be delivered •
Brain particularly sensitive – PO2 3040 mmHg =seizures & coma •
Other symptoms –nausea, muscle twitching, dizziness, visual disturbances, disorientation, irritability •
For metabolism, molecular O2 must be converted into O2 free radicals = highly reactive, and potentially lethal compounds if not controlled
What are the effects of diving on CO2 and what is a complication it could cause
PaCO2 determined by metabolic rate and VA •
Diving in itself does not cause problems with CO2 – depth does not cause PACO2 provided diver exhales CO2 normally – normal VA
• However, PACO2 can occur if CO2 builds up in the “dead space” of the SCUBA apparatus and is re-breathed •
Divers can tolerate a PACO2 ~ 80mmHg – up to 10-fold ↑ in respiratory volume – beyond 80mmHg, respiration begins to fail – respiratory acidosis, lethargy, anaesthesia
What are nitrogen 3 effects at high pressures
Nitrogen is highly lipid solubleand can cause varying degrees of narcosis
Nitrogen is soluble is body tissues (especially lipids) and can cause bubble formationon decompression
Nitrogen has a high density at high pressure, results in hindrance to breathing
What is narcosis
N2 is highly lipid solubleand can cause varying degrees of narcosis– similar to alcohol intoxication –“raptures of the deep
What is decompression illness
If the divers comes to the surface too quickly (i.e. ↓ pressure rapidly) volume of N2 will ↑ quickly and N2 bubbles can develop in body fluids (intra- or extracellular) •
Bubbles may form in tissues and blood – may block small vessels – may not occur for several hours •
Coalescing bubbles may block larger vessels – tissue ischaemia and tissue death •
Most people will suffer pains in joints and muscles
why can you not fly after you dive
what does high altitudes do to barometric pressure and inhaled O2 and what effect does this have on CO2
decreases them
↓PiO2 ↓ PAO2 & ↓PaO2
i is inspired
•Decrease in inspired oxygen =Hypoxia •PaCO2 due to hypoxic driven hyperventilation
what are 5 adaptions that your body undergoes if you are acclimatised to high altitude
Large (x5) in pulmonary ventilation
red blood cells (polycythemia)
vascularity in tissues (angiogenesis)
diffusing capacity in lungs
ability of tissues to use O2 ( mitochondria, mitochondrial enzymes)
what are the effects of hypoxia at high altitudes (DDLMM
– Decreased mental proficiency
–decreased judgment memory and motor performance –
Drowsiness –
Lassitude –
Mental and muscle fatigue –
Nausea (occasionally) & Euphoria (sometimes)
what is khumbu cough
•Inhaling subzero air causes extreme irritation of bronchi & respiratory membranes causing a drypersistent cough •
Can restrict breathing, result in torn chest muscles or broken ribs •
Damaged epithelial lining can slough off & be coughed up
difference between acute mountain sickness and chronic mountain sickness
Acute mountain sickness (AMS)– occurs in some people who rapidly ascend to high altitudes – can be fatal if not given O2 or removed to lower altitude – more severe forms: cerebral oedema (HACE) and pulmonary oedema (HAPE) •
Chronic mountain sickness (CMS) – occasionally occurs in people who stay at altitude for a long time – excessively increased red cell mass, pulmonary hypertension, myocardial hypertrophy – leads to congestive heart failure
what are the 3 drugs for mountain sickness and what do they do
• Diamox (Acetazolamide) – respiratory stimulant at altitude – inhibits carbonic anhydrase, ↓reabsorption of HCO3- in PCT thus facilitates renal loss of HCO3-. By ↓ respiratory alkalosis induced by hypocapnia, it helps to facilitate ↑ ventilation by mitigating hypocapnic loss of central respiratory drive •
Dexamethasone – decreases oedema – glucocorticoid agonist = inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in oedema •
Nifedipine – decreases pulmonary artery pressure – Ca2+ slow-channel blocker, inhibits influx of Ca2+ into vascular smooth muscle causing ↓vascular resistance
what is HAPE
• Fluid build up in the lungs due to ↑ pulmonary artery pressure (result of pulmonary hypoxic vasoconstriction across entire lung) •
Decrease SaO2 results in cyanosis, impaired cerebral function and death •
Symptoms = shortness of breath, fatigue, weakness, persistent productive cough, confusion and irrational behaviour •
Immediate descent needed •
Nifedipine & Dexamethasone • Supplemental O2 and Gamow Bag (simulates a lower altitude
